Abstract
Regulation of adhesion is a ubiquitous feature of living cells, observed during processes such as motility, antigen recognition, or rigidity sensing. At the molecular scale, a myriad of mechanisms are necessary to recruit and activate the essential proteins, whereas at the cellular scale, efficient regulation of adhesion relies on the cell’s ability to adapt its global shape. To understand the role of shape remodeling during adhesion, we use a synthetic biology approach to design a minimal experimental model, starting with a limited number of building blocks. We assemble cytoskeletal vesicles whose size, reduced volume, and cytoskeletal contractility can be independently tuned. We show that these cytoskeletal vesicles can sustain strong adhesion to solid substrates only if the actin cortex is actively remodeled significantly. When the cytoskeletal vesicles are deformed under hypertonic osmotic pressure, they develop a crumpled geometry with deformations. In the presence of molecular motors, these deformations are dynamic in nature, and the excess membrane area generated thereby can be used to gain adhesion energy. The cytoskeletal vesicles are able to attach to the rigid glass surfaces even under strong adhesive forces just like the cortex-free vesicles. The balance of deformability and adhesion strength is identified to be key to enable cytoskeletal vesicles to adhere to solid substrates.
Highlights
Giant unilamellar vesicles have proven to be an excellent model system to study basic processes of cellular adhesion [1,2,3,4,5,6,7]
Our model system is a giant unilamellar vesicle containing a cross-linked actin cortex anchored to its inner leaflet
The His-tagged anillin is responsible for both cross-linking the actin and coupling the actin network to the Ni-NTA lipids that are incorporated into the membrane
Summary
Giant unilamellar vesicles have proven to be an excellent model system to study basic processes of cellular adhesion [1,2,3,4,5,6,7]. In going from an unbound state to a bound state, the vesicles undergo significant shape transformations [11,12,13,14] This adhesion-induced shape transformation has been successfully explained by free energy minimization in the framework of the Helfrich theory of elastic cells [15,16]. What has already been established is that binding the cortex to the membrane causes dampening of membrane fluctuations and increases the membrane tension for both cells and vesicles [17,18]. How this would influence the adhesion process is yet to be explored
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